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DMD 5247 > Blood Vessel Pathology > Flashcards

Blood Vessel Pathology Flashcards

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1
Q

vessels most affected by atherosclerosis

A
  • abdominal aorta
  • coronary arteries
  • popliteal arteries
  • carotid arteries
  • vessels of the circle of Willis
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2
Q

contents of a plaque

A

fibrous cap
necrotic center
media

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3
Q

step 1

A

chronic endothelial injury

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4
Q

high blood pressure damages the endothelium and activates:

A

inflammation

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5
Q

high blood pressure promotes:

A

turbulent flow in a blood vessel

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6
Q

this turbulent flow is particularly evident in areas of:

A

branching or constriction of the blood vessel

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7
Q

what effect does endothelial damage have on cholesterol invasion and clot formation

A

increases the likelihood

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8
Q

step 2

A

endothelial dysfunction

monocyte adhesion and emigration

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9
Q

step 3

A

macrophage activation

smooth muscle recruitment

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10
Q

step 4

A

leukocytes and smooth muscle cells engulf lipid

hyperlipidemia is a primary player in the etiology

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11
Q

step 5

A

smooth muscle proliferation
collagen and extracellular lipid deposition
(complicated plaque)

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12
Q

major non-modifiable risk factors

A

age
gender
genetics

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13
Q

major modifiable risk factors

A

lifestyle
cigarette smoking
diabetes
inflammation

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14
Q

complications of atherosclerosis

A

stenosis
thrombosis/embolus
aneurysm
calcification

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15
Q

what must occur for cholesterol to be a problem

A

oxidation

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16
Q

major steps of atherosclerosis

A
  1. LDL enters the intima through the inner endothelium
  2. Intimal LDL is oxidized into pro-inflammatory lipids
  3. Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across the endothelium
  4. monocytes differentiate into macrophages which then consume large amounts of LDL: forming foam cells
  5. foam cells release cytokines: that encourage atherosclerosis
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17
Q

How many patterns or types of LDL cholesterol are there

A

2

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18
Q

Type A cholesterol

A

Large, less dense

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19
Q

Type B cholesterol

A

small, more dense

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20
Q

Which one more easily penetrates the endothelium

A

Type B

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21
Q

Risk factors for pattern B

A

genetics
oral contraceptives
diet

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22
Q

what effect does increased glutathione activity have on atherosclerotic development?HMG

A

slows the atherosclerotic development

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23
Q

Statins

A

HMG-CoA Reductase inhibitors

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24
Q

most circulating cholesterol is synthesized de novo

A

80% in the liver
10% in the intestine
5% in the skin

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25
HMG-CoA reductase inhibitors
May prolong life in those with previous cardiovascular event history provide very little primary protection increases risk of diabetes other side effect
26
side effects of statins
``` increases the risk of diabetes kidney failure liver failure muscle pain rhabdomyolysis: muscle break down --perhaps a function of reduced ubiquinone(Coenzyme Q10) ```
27
What does reduced ubiquinone (Coenzyme Q10) cause
``` Myopathy: muscle weakness and pain reduced mitochondrial function oxidative stress intima media thickness increase cataracts ```
28
What does cholesterol do that is so important
``` cell membranes steroid synthesis bile salts vitamin D ubiquinone ```
29
hypertension
affects 25% of the population | asymptomatic until later
30
what are the different types of hypertension
benign and malignant
31
benign hypertension
essential: 95% of cases | secondary
32
essential benign hypertension
- primary hypertension - idiopathic - appears to be a mix of genetic and environmental factors - erroneously assumed to result from weight gain
33
secondary benign hypertension
-resulting from structural, renal, or endocrine defects
34
structural defect causing secondary benign hypertension
aortic coarctation
35
renal defect causing secondary benign hypertension
renal artery stenosis
36
endocrine defect causing secondary benign hypertension
adrenocortical hyperfunction
37
benign hypertension increases risk of:
- atherogenesis - aortic dissection - stroke
38
hypertension causes what types of small blood vessel disease
hyperplastic arteriosclerosis | hyaline arteriosclerosis
39
malignant hypertension
lethal in 1-2 years if left untreated
40
malignant hypertension usually accompanies:
- renal failure - retinal hemorrhages - papilledema (blurred disk margins)
41
RAAS Dysfunction
- insulin increases kidney sodium reabsorption - insulin increases aldosterone secretion - a very slight increase in plasma insulin is capable of eliciting an antidiuretic effect
42
Enhanced growth factor activity
receptors in capillary endothelial cells - vascular cells are esponsive to insulin - hypertrophy of the vascular wall leads to narrowing of vascular lumen
43
SNS
insulin causes a dose-related increas in norepinephrine release subsequent increase in pulse and blood pressure
44
dyslipidemia
``` reduced HDL increased VLDL increased LDL -pattern B Increased triglycerides ```
45
nitric oxide
NO reduces blood pressure: made from L-arginine insulin increases NO production NO is a potent vasodilator
46
aneurysm
localized abnormal vessel dilation
47
true aneurysm
involves all three layers
48
false aneurysm
hole covered with a hematomq (extravascular connective tissue)
49
causes of an aneurysm
- caused by atherosclerosis - wall degeneration - trauma - congenital defects (Marfan Syndrome) - infection
50
aortic dissection
aortic wall tears and blood pours into wall
51
Type A1 of aortic dissection
originates in ascending aorta, propagates to the ascending aorta and often beyond it distally
52
Type A2 of aortic dissection
Originates in ascending aorta and is confined to the ascending aorta
53
Type B3 of aortic dissection
originates in the descending aorta, rarely extends proximally but will extend distally
54
aortic dissection can be caused by
hypertension | trauma
55
Vasculitis
inflammation of blood vessels
56
Giant-cell artheritis
most common vasculitis chronic granulomatous inflammation of the large to small arteries accompanied by fever, headache, vision loss treatment: corticosteroids
57
takayasu arteritis
granulomatous vasculitis of the aortic arch severe narrowing in upper extremities ocular disturbances
58
polyarteritis nodosa
different stages coexist in the same artery varied symptoms fatal if untreated, but steroids are curative
59
wegener granulomatosis
lung granulomas, renal disease, vasculitis T-cell mediated hypersensitivity fatal if untreated within a year c-ANCA positive
60
churg-strauss syndrome
similar to wegener but more related to alergies and asthma, without the renal disease
61
microscopic poly angitis
widespread necrotizing vasculitis of smaller vessels antibody response to the drug or bug neutrophils heavily present in vessels possibly type 3 hypersensitivity removing offending agent usually resolves the problem
62
tumors
hemangioma glomus tumor kaposi sarcoma angiosarcoma
63
capillary hemangioma
skin, oral mucosa, sometimes organs | strawberry type present at birth, regresses
64
cavernous hemangioma
``` organs, sometimes skin cosmetic problem (unless brain) ```
65
pyogenic granuloma
rapidly growing red nodule on skin, in mouth | microscopically resembles granulation tissue
66
glomus tumor
benign but painful arise from glomus body cells distal digits, especially under fingernails excise
67
kaposi sarcoma
``` low-grade malignancy of endothelial cells 4 forms -chronic -african -transplant-associated -AIDS associated ``` clinical course varies: chronic is the best prognosis excise
68
angiosarcoma
high-grade malignancy of endothelial cells often in skin, soft tissue, breast, liver arsenic and PVC increase risk covers a spectrum from well-differentiated to anaplastic metastasize rapidly

DMD 5247 (13 decks)

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